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1 an adenoviral vector expressing human blood coagulation factor IX.
2 xicity and promote the delivery of the human coagulation factor IX and alpha-galactosidase genes into
4 in patients with haemophilia B (defective in coagulation factor IX) and the Marfan syndrome (defectiv
5 is caused by the absence of functional blood coagulation factor IX, and is an excellent candidate for
6 gene on the X chromosome that encodes blood coagulation factor IX, and is predicted to alter RNA spl
7 o demonstrate a polymorphism of human plasma coagulation factor IX antigen in double antibody solid-p
8 g-term expression (>5 months) of human blood coagulation factor IX at levels that were therapeutic in
10 We have used gene targeting to develop a coagulation factor IX-deficient (factor IX-knockout) mou
11 lia B is caused by the absence of functional coagulation factor IX (F.IX) and represents an important
12 sociated viral (AAV) vector expressing blood coagulation factor IX (F.IX) can result in long-term exp
15 g disorder hemophilia B [deficiency in blood coagulation factor IX (F.IX)] by gene replacement therap
17 at antigenic epitopes derived from an ARF in coagulation factor IX (F9) cDNA can induce CTL reactivit
18 n particular, we target a promoterless human coagulation factor IX (F9) gene to the liver-expressed m
19 d efficient induction of immune tolerance to coagulation factor IX (FIX) by direct intramuscular inje
20 emonstrated induction of immune tolerance to coagulation factor IX (FIX) by hepatic adeno-associated
22 associated viral (AAV) vector encoding blood coagulation factor IX (FIX) into skeletal muscle results
23 d mice with combined deficiencies of Plg and coagulation factor IX (fIX) or XI (fXI) to determine the
24 safety of recombinant fusion protein linking coagulation factor IX (FIX) with albumin (rIX-FP) which,
29 onsidering the enzymatic domain of activated coagulation factor IX (FIXa) is homologous to those of t
30 ient to maintain therapeutic levels of human coagulation Factor IX for more than six months in mice u
32 are the result of missense mutations in the coagulation factor IX gene and defective circulating fac
33 cin resistance marker gene (neo) and a human coagulation factor IX genomic construct designed for exp
35 tion of immune tolerance to a secreted human coagulation factor IX (hF.IX) antigen by adeno-associate
37 arried out a systematic study on human blood coagulation factor IX (hFIX) and anti-coagulant protein
42 closely related fragment, the Gla domain of coagulation factor IX, the structure of which had previo
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